We have discovered that scattered light intensity fluctuations (SLIF) are present in isolated rat ventricular muscle even under conditions formerly considered to be quiescent. Subsequent experiments indicated that SLIF are highly dependent on calcium loading of the cell and could be reversibly terminated (1) by maintaining constant calcium concentration in the myofilament space in skinned fibers or (2) in intact fibers by caffeine. These results were interpreted to indicate that cellular myoplasmic calcium concentration oscillates in diastole, producing motion of the myofilaments, which modulates the laser beam and results in SLIF. This myofilament motion which is asynchronous within a cell, and among cells, results in a small degree of diastolic force or "tone" in the muscle. Additional experiments have demonstrated SLIF in atrial, ventricular, and conduction tissues in a range of mammalian species including man and indicate the universality of this phenomenon in excitable cardiac tissues. We have directly demonstrated these calcium oscillations utilizing intracellular injects of the chemiluminescent protein, aequorin and modeled the effect of heterogeneous calcium oscillation on tonic force. We have also demonstrated the presence of SLIF in the intact perfused heart and have shown that it covaries with calcium-dependent tone. In our most recent studies we have determined the specific characteristics of myofilament motion that cause SLIF. We have also shown that ischemia suppresses spontaneous calcium release and reperfusion exacerbated it.